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HSC expansion requires multiple interacting cytokines that influence growth, differentiation and apoptosis, making this a very complex system to optimize.
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Systemic lupus erythematosus (SLE) is a complex autoimmune disease of unknown etiology that involves multiple interacting cell types driven by numerous cytokines and autoimmune epitopes.
Multiple interacting systems can be designed with separation of concerns.
In social organisms, phenotypes are influenced by the genotypes of multiple interacting individuals.
Furthermore, TNF- α can interact with multiple cytokines to produce extensive effects.
There are multiple interactions between pro-inflammatory cytokines and glucocorticoids.
There are, in fact, many more levels of complexity; with multiple cytokines and multiple U-shaped curves that interact, it may be impossible to predict whether a specific anti-cytokine therapy will benefit or harm a given patient, especially as the cytokine profiles change during the course of the disease.
Capable of rapid dynamism and motility, they also synthesize and release multiple cytokines, chemokines, neurotrophic factors, and neurotransmitters that allow them to interact with multiple CNS cell types and exert cytotoxic or cytoprotective effects depending on the tissue context [23].
As cells in vivo likely encounter multiple cytokines simultaneously, we assessed the effect of multiple cytokines on Mcl-1 dependence.
High expression of multiple cytokines suggests that tumour angiogenesis is activated by multiple pathways.
Multiple factors (hormones, cytokines, growth factors, and vitamins) have been described as interacting with the OPG/RANKL pathway.
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